In human AD, LRP1, which is a primary receptor for the clearance of amyloid-β, is downregulated with an increase in oxidative stress (Deane et al., 2004; Donahue et al., 2006; Sagare et al., 2007; Miller et al., 2008; Owen et al., 2010; Halliday et al., 2016); as a result, the transport of Aβ from the brain becomes reduced and leads to amyloid-β accumulation in the brain (Deane et al., 2004, 2008; Storck et al., 2016). Here, LRP1 is linked to Alzheimer disease.